Diet-Induced Gut Dysbiosis and Leaky Gut Syndrome

J Microbiol Biotechnol. 2024 Apr 28;34(4):747-756. doi: 10.4014/jmb.2312.12031. Epub 2024 Feb 1.

Abstract

Chronic gut inflammation promotes the development of metabolic diseases such as obesity. There is growing evidence which suggests that dysbiosis in gut microbiota and metabolites disrupt the integrity of the intestinal barrier and significantly impact the level of inflammation in various tissues, including the liver and adipose tissues. Moreover, dietary sources are connected to the development of leaky gut syndrome through their interaction with the gut microbiota. This review examines the effects of these factors on intestinal microorganisms and the communication pathways between the gut-liver and gut-brain axis. The consumption of diets rich in fats and carbohydrates has been found to weaken the adherence of tight junction proteins in the gastrointestinal tract. Consequently, this allows endotoxins, such as lipopolysaccharides produced by detrimental bacteria, to permeate through portal veins, leading to metabolic endotoxemia and alterations in the gut microbiome composition with reduced production of metabolites, such as short-chain fatty acids. However, the precise correlation between gut microbiota and alternative sweeteners remains uncertain, necessitating further investigation. This study highlights the significance of exploring the impact of diet on gut microbiota and the underlying mechanisms in the gut-liver and gut-brain axis. Nevertheless, limited research on the gut-liver axis poses challenges in comprehending the intricate connections between diet and the gut-brain axis. This underscores the need for comprehensive studies to elucidate the intricate gut-brain mechanisms underlying intestinal health and microbiota.

Keywords: Diet; intestinal dysbiosis; leaky gut syndrome; microbiota; tight junction proteins.

Publication types

  • Review

MeSH terms

  • Bacteria / classification
  • Bacteria / metabolism
  • Brain-Gut Axis / physiology
  • Diet* / adverse effects
  • Dysbiosis* / microbiology
  • Gastrointestinal Microbiome* / physiology
  • Gastrointestinal Tract / microbiology
  • Humans
  • Inflammation
  • Liver / metabolism